Week 7 Flashcards
What is acute coronary syndrome?
Range of symptoms / conditions associated with sudden reduced blood flow to the heart
Excessive sweating
diaphoresis
Commonest cause of ACS
Rupture of atherosclerotic plaque
Stable vs unstable plaque
Stable - small necrotic core (With lipid content) and think fibrous cap Unstable - thick necrotic core, thin fibrous cap
Stable vs unstable angina
stable - demand ischemia, no infarct, normal ECG, breathlessness/pain upon exertion unstable - supply ischaemia, no infarct, thrombus forms but occlusion is only partial, may have abnormal ECG (inverted T, ST depression)
NSTEMI vs STEMI
NSTEMI - Subendocardial infarct, plaque rupture, partial occlusion , cardiac enzymes in the blood, may have abnormal ECG (inverted T, ST depression), some damage STEMI - XXX
Clinical presentation of ACS (5)
Chest pain, can radiate to left shoulder, at rest / exertion (Squeezing, heaviness) Sweating Shortness of breath dizziness anxiety (sense of impending doom)
What blood tests do you for suspected MI? (6) And why
Troponin - sign of heart cell death (not present in unstable angina) FBC - to check for anaemia / haemoglobin CKMB - cardiac enzyme Lipid profile - cholesterol Glucose - to check for diabetes D-dimer - to check for clotting (can help rule out clotting)
Investigations for suspected MI
ECG Bloods - cardiac enzymes, other tests CXR Echocardiogram
How long does it take for troponin to return to normal after MI?
up to 2 weeks
What are we looking for with echo?
Resting wall cardiac abnormalities
Immediate management of STEMI in hospital (4)
MONA Morphine (possibly with anti-emetic) Oxygen (below 90%) Nitroglycerine (vasodilator) ASA - ticagrelor or clopidogrel
Management of suspected STEMI out of hospital (what to do depending on distance from hospital, what type of hospital)
120 min from tertiary centre, go directly (give GTN spray and aspirin chewed) If more than 120 min, give thrombolytics (and still go to tertiary centre)
How do you score patients with ACS?
Risk stratify using Grace Score
What is long term treatment plan for MI patient post-discharge? (4 drugs)
Statins - stabilise clot and reduce blood cholesterol ACE inhibitor - prevents remodelling of heart (can be used in patients w/o hypertension for this) Beta blockers - to decrease heart rate so heart can rest to heal Dual antiplatelet - especially after angio (aspirin and ticagrelor)
What are the secondary prevention methods recommended post MI? (4)
Reduce alcohol consumption Regular physical activity (slow, post recovery) Smoking cessation Weight management
What is health promotion?
Broad promotion of wellness, good health (broader and distinct from prevention)
Describe risk as a clinical tool
It is a statistical entity that gives you an odds ration based on statistics - it is not predictive of individual outcomes
Important considerations when considering a particular patient and risk
Epidemiology implies statistical relationships are causal for individuals Focus on measurable factors of ‘risk’ can result in neglecting less measurable social/cultural contexts
Describe the social construction of risky behaviour
The context around the behaviour - variable thoughts about a particular risk depending on their position within society / their individual position in society People have their own rational reasons to engage in risky behaviour
What is concordance?
Beyond compliance (you tell patient), you work with patient to understand why they are making changes Mutual respect
Explain the notion of risk in the context of health promotion and disease prevention strategies
Less likely to be examined
Assess relative efficacy of socio-cultural theories of risk perception and ‘risky’ behaviour
Likely to be examined
Describe the process of cardiac myocyte contraction
Action potential generated at AV node Current TRAVELS through myocytes via gap junctions ACTIVATES L type calcium channels (resulting in calcium moving into cytoplasm) Calcium binds to ryanodine (which causes more calcium to ENTER) Calcium BINDS to Troponin C (which causes CONFORMATIONAL CHANGE) Actin and myosin BIND Pulls actin filaments Then calcium leaves cells, dissociates from Toponin C, end of contraction
Nodal action potential - in which cells, axis, what flows in and out of cell?
Pacemaker /nodal cells Membrane potential (mV) / time Na+, Ca2+ IN K+ OUT
In myocyte action potential, why is there a prolonged action potential caused by calcium influx?
To ensure heart has sufficient time to contract / relax
What are the main ions involved in cardiac contraction and conduction?
Sodium, calcium, potassium (and chloride)
What is the function of T tubule?
Allows currents to travel deep into the muscle cell
Describe sarcoplasmic reticulum in myocyte cell
Intracellular storage of calcium Ryadine receptor on surface (where calcium binds) Releases more calcium
Normal function of troponin
Prevent contraction of muscle cells (through binding of actin and myosin) unless they are stimulated by current The calcium causes change in troponin, which gets it out of the way to allow contraction
What drives the automaticity of the heart?
xxx
Changes in preload, and implication of treating with fluid
Preload reserve, fluids will help increase stroke volume Normal preload, fluids won’t help No preload reserve, heart failure,
Principles of Frank Starlings’s Law of the Heart (3)
If you Increase filling of the heart Stretch of the heart and increase the number of bonds between myosin/action you increase the force of contraction
What is the most important determinant of cardiac output in the healthy heart?
Preload (the filling)
What determines venous return? (3)
Mean systemic filling pressure Right atrial pressure Resistance
Cardiac output depends on… (two concepts)
HR x stroke volume Pressure difference between arterial system and venous system
How do you keep venous pressure high? (2)
More volume Venoconstriction (by giving something like adrenaline)
What alters preload? (2)
Too much volume OR Sepsis (venodilation) - treat with fluids or venoconstriction
How do you treat chronic / worsening heart failure?
Decrease preload - venodilators Try to increase cardiac contractility with some medicines
What is a prospective cohort study?
A group of people with different exposures are followed over time to see if they develop disease / outcome
What are the strengths of cohort study? (5)
Exposure measured BEFORE disease develops Information on SEVERAL PARAMETERS - relative risk, incidence, attributable risk Can look at SEVERAL EXPOSURES / OUTCOMES at the same time Allow TEMPORAL SEQUENCE Potential for NESTED CONTROL studies
What are the Bradford-Hill criteria? (9)
Strong - high relative risk Independent - not the result of confounding Dose response Temporal sequence - exposure, then outcome Consistent Specific Reversible Biological plausibility - do mechanisms make sense Analogy - parallels with other disease models
Primary, secondary, tertiary prevention - definitions in CHD
Primary - prevention Secondary - early disease, minimisation and preventing recurrence Tertiary - Late stage CHD, limit progression
Primary prevention in CHD - 3 strategies
Removal of causal exposure Enhancement of host resistance Interfere with disease pathogenesis
Secondary prevention in CHD - 3 strategies
Encourage early identification of disease Encourage early preventative/treatment measures in diagnosed cases Removal of causal exposure
Tertiary prevention in CHD - 2 strategies
Ensure effect treatment Removal of causal exposure
What are the three scenarios for widescale CHD prevention?
Secondary prevention - focus on people who have already had issues (due to high risk of recurrence), meds, lifestyle changes Primary prevention - start with high risk people (clinical approach Primary prevention- reduce risk in whole population (public health approach
What is the ‘polypill’ strategy?
Give everyone over 55 a mixed pill that contains a low dose of statin, aspirin, beta blocker, ace inhibitor Population prevention
What are key aspects of population strategy of CHD prevention? (3)
Population diet changes Cigarette smoking restrictions Encouraging physical activity
What is the prevention paradox?
xxx
What causes the S3 heart sound?
S3 caused by incomplete relaxation of ventricle (during passive phase of diastole)
When is bypass better than PCI?
Diabetic patients, LAD, LCA (but depends on age, number of blockages)
